Sarcoplasmic reticulum (SR) plays an important role in cardiac relaxation and tension development by its ability to sequester and release calcium, although previous investigations have suggested that impaired calcium accumulating capacity of the SR accompanies the decrease in cardiac performance during hypertrophy and failure. The precise mechanisms involved are not known and will be the focus of the proposed studies. Different models of cardiac hypertrophy will be used: (a) aortic constriction; (b) aorto-caval shunt; (c) exercise-induced; and (d) thyroxine-induced. Mechanical performance of the heart at different stages of cardiac hypertrophy will be correlated with calcium transport by SR. The following parameters will be examined: (a) calcium uptake, binding and Ca ions-ATPase; (b) chemical composition of SR; (c) partial reactions of ATP hydrolysis; (d) ionophoric ability of ATPase; (e) cyclic AMP-induced SR phosphorylation. It is hoped that these studies will provide insight into the pathogenesis of heart failure.